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Spaska Stanilova

Trakia UniversityBulgaria

Dr Spaska Angelova Stanilova started her career in Medical Biology and received her PhD in Immunology at Higher Medical Institute in 1991. She is currently a full professor of Molecular Biology and Dcs in Immunology, and Head of Department of Molecular Biology, Immunology and Medical Genetics at the Faculty of Medicine, Trakia University. At the department, she leads the Molecular Immunology research unit at the crossroad of genetics and immune regulation. Their main research goals are to gain an insight into the molecular mechanisms of gene expression with an emphasis on implication of cytokine gene polymorphisms and intracellular signaling in immune mediated and cancer diseases. Dr Stanilova is a member of the European Federation of Immunological Society and has reviewed for several scientific journals.

1books edited

3chapters authored

Latest work with IntechOpen by Spaska Stanilova

Autoimmune disorders are known to affect a substantial number of people worldwide, demonstrating a gender bias and are the second largest cause of chronic illness. Recently, the attention has been focused on lifestyle changes as a major factor in the rise of autoimmune disease frequency. The two sections of this book are focused on the new opportunities for moving research forward, leading to a new approach to prevention and treatment of autoimmune diseases. A better understanding of the mechanisms of gene expression and triggering signaling pathways, which is involved in autoimmune pathogenesis simultaneously with current data for the interaction of microbiota with human immune system, will help to better understand the immune imbalance implicated in autoimmunity.

Cells of the innate and the adaptive immune system have been identified as the key players in inflammatory bowel disease (IBD) pathogenesis, and the cytokines are central components of the inflammatory pathways that take place in the gut mucosa during the active and chronic phases of IBD. The effector cell response is largely determined by the type of cytokines that predominate in the intestinal mucosa. Here we describe the main cytokine players in intestinal inflammation during IBD—related to innate immune responses (tumor necrosis factor α—TNFα), TNF-like cytokine 1A, IL-8), and related to adaptive immune responses—Th1 (IL-1β, IL-18, IFNγ, IL-12), Th2 (IL-4, IL-5, IL-13, IL-11, IL-33), Th17 (IL-17A, IL-17F, IL-21, IL-22, IL-25, IL-27), cytokines required for Th17 development (IL-6, TGFβ, IL-23), anti-inflammatory cytokine IL-10 and Tregs along with IL-2. Recently described innate lymphoid cells (ILCs) could also be potential sources of IFN-γ, TNF, IL-5, IL-13, IL-17, and IL-22. The effects of cytokines in the gut are described in conjunction with the clinical implication and available biologic therapy. The data in the literature and our own results make us believe that in order to achieve immune homeostasis in the gut, pro-inflammatory and anti-inflammatory responses that define the mucosal cell immunophenotype should achieve balance.